Members of the natriuretic peptide family are hormones that regulate body fluid homeostasis. Atrial natriuretic peptide (ANP) is secreted by atrial myocytes in response to increased intravascular volume. Once ANP is in the circulation, its effects are primarily on the kidney, vascular tissue, and adrenal gland, in which its actions lead to the excretion of sodium and water by the kidneys and a decrease in intravascular volume and blood pressure. BNP also is of myocardial cell origin, and like ANP, it circulates in human plasma. BNP is natriuretic, rennin inhibiting, vasodilating, and lusitropic. The main circulating and storage form of BNP is a 32 amino acid peptide with a ring structure. Physiological actions of BNP are mediated through a guanylate cyclase-linked receptor, natriuretic peptide receptor A (NPR-A). Clearance of BNP is promoted by a NPR-C receptor that removes it from the circulation. BNP also is degraded through enzymatic cleavage by neutral endopeptidase. C-type natriuretic peptide (CNP) is of endothelial cell origin and functions as a vasodilating and growth-inhibiting peptide. Dendroaspis natriuretic peptide (DNP) is similar in structure to ANP, BNP, and CNP, and is isolated from the venom of Dendoaspis angusticeps or green mamba snake.
ANP and BNP are increased in the plasma and heart during congestive heart failure in humans, and exert cardiorenal protective actions in addition to serving as serum markers for ventricular dysfunction. Epidemiological evidence indicates that at least 3% of the adult population above the age of 45 may have ventricular systolic dysfunction and 52% may be asymptomatic.